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FHB Hormone/Repro > 75 - HPA axis and adrenal gland > Flashcards

75 - HPA axis and adrenal gland Flashcards

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1
Q

In what hypothalamic nucleus is corticotrophin-releasing hormone/factor (CRH/CRF) release from?

A

PVN

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2
Q

What CRH/CRF stimulate the release of?

A

ACTH release from corticotropes in anterior pituitary

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3
Q

What is the target gland of ACTH?

What is produced?

A
  • Adrenal cortex

- Cortisol

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4
Q

What triggers CRH release?

What are some specific eg’s?

A

Stress

- Emotional, chemical (e.g. drugs of abuse), physical (e.g. temperature)

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5
Q

How many AA’s is CRH?

A

41 AAs

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6
Q

Is CRH produced by parvo or magnocellular neurons of the PVN?

A

Parvocellular (ant pit)

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7
Q

What is the pattern of CRH release from the PVN?

A

Pulsatile (results in episodic release)

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8
Q

What is the half-life of CRH?

A

~5 min

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9
Q

What type of receptor does CRH bind?

A

GPCR

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10
Q

What are the names of the 2 CRH receptors?

A

CRH R1 and CRH R2

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11
Q

Regarding CRH receptors, which binds CRH in ant pit w/higher affinity?
Which binds w/higher affinity to urocortin?

A
  • CRH R1

- CRH R2

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12
Q

What is the 2nd msger system of CRH after it binds its GPCR?

A

GPCR -> GDP -> GTP -> AC -> PKA -> L-type Ca2+ channels -> Ca2+ in -> ACTH release

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13
Q

What hormone acts synergistically w/CRH to increase amplitude of ACTH release from the ant pit?

A

AVP

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14
Q

What is the name of the receptors that cortisol binds to negatively feedback on both the hypothalamus and anterior pituitary?

A

Nuclear steroid hormone glucocorticoid receptor (GR)

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15
Q

What hormones does cortisol inhibit the synthesis and release of when it binds GRs on the PVN?

A

CRH and AVP

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16
Q

From what gene does cortisol come from?

A

POMC (pro-opiomelanocortin), along w/a number of other hormones that are important for pregnancy and fetal development

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17
Q

What are the names of the 2 receptors to which ACTH binds?

A

melanocortin 1 and 2 receptors (MC1R, MC2R)

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18
Q

Which of the 2 receptors that ACTH binds (MC1R or MC2R) have a higher affinity for ACTH?
Where is the other receptor found, which binds ACTH w/lower affinity?

A
  • MC2R: Adrenal gland

- MC1R: Skin

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19
Q

Because ACTH binds the MC1R in the skin, very high levels of ACTH can lead to ____________ of the skin.

A

Hyperpigmentation (via melanin synthesis/dispersal)

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20
Q

How is small-lung cell carcinoma related to the stress HPA axis?

A

It’s a non-pituitary tumor that autonomously makes ACTH.

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21
Q

What are the immediate, subsequent, and long-term effects of ACTH binding its high-affinity MC2R receptor in the adrenal gland?

A

IMMEDIATE:
- Increased cholesterol esterase, decreased CE synthetase, increased cholesterol xport to mito, increased cholesterol binding to P450scc, increased pregnenolone production, increased StAR (all to make steroid hormones)
SUBSEQUENT
- Increased gene TS of P450scc/c17/c11, adrenoxin, LDL and HDL receptors
LONG-TERM
- Increased size and functional complexity of organelles
- Increased size and number of cells

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22
Q

The adrenal cortex derives from the (endo/meso/ecto-derm).

A

Mesoderm

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23
Q

The adrenal medulla derives from ______________.

A

Neural crest (it’s basically modified sympathetic postganglionic neurons)

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24
Q

(adrenal cortex or medulla?)

Steroid hormones are made in the ___________, while catecholamines are processed in the ____________.

A

cortex

medulla

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25
Starting from the capsule and moving in, name the 4 layers of the adrenal gland.
Cortex: "GFR" (80-90%) 1. Zona glomerulosa (15%) 2. Zona fasciculata (65-80%) 3. Zona reticularis (
26
What hormones are found in the zona glomerulosa?
Mineralocorticoids (aldosterone)
27
What hormones are found in the zona fasciculata?
Glucocorticoids (cortisol)
28
What hormones are found in the zona reticularis?
Weak androgens (DHEAS)
29
What hormones are synthesized in the medulla?
NE/E
30
Why do you see lipid droplets on histological sections of the adrenal cortex?
Steroidogenic cells need cholesterol to make steroids
31
What is the name of the type of cell in the medulla that makes NE/E?
Chromaffin cells
32
Explain the adrenal cortex and medulla blood supply. (2 things)
Dual blood supply - There are 2 plexi that come into the cortex; this will come down and bath the medulla in corticosteroids (important for NE -> E conversion) - There is also a separate artery that goes straight to medulla
33
What are glucocorticoids bound to in blood? (2 names + generic)
CBG/transcortin (90%) | - Also 7% to albumin
34
In what manner/pattern are glucocorticoids released?
Circadian manner, peaking around 8AM
35
Cortisol binds w/high affinity to what 2 receptors in the cytoplasm?
- Glucocorticoid receptor (GR) | - Mineralocorticoid receptor (MR)
36
Where are MRs found? Where are GRs found?
GR are everywhere, MR are restricted to where aldosterone acts. (recall, CRH and AVP closely related)
37
To which "family" does CBP/transcortin belong?
Serpin family: serine protease inhibitor, NOT a protease inhibitor
38
How does estrogen affect CBP during pregnancy, and how does this affect cortisol?
Decreases it, increasing serum cortisol
39
Besides estrogen, what medical conditions can decrease CBP?
- Shock - Severe infection - Hepatitis
40
If cortisol is mostly bound by CBP, how could this alter the effects of another major hormone?
Since cortisol binds MRs and GRs, there will be less cortisol in the blood to compete w/aldosterone for binding to the MRs
41
What type of receptor of GR?
Nuclear steroid receptor | - Ubiquitously expressed in most tissues
42
What occurs when cortisol binds GR, mechanistically?
Cortisol binding dissociates GR from chaperone proteins (ie HSPs) in cytoplasm - Cortisol:GR complex translocates to nucleus and acts as TS factor on gene promoters
43
Cortisol is a pleiotropic hormone. What are some of its affects on muscle?
Maintain m. fcn/decrease m. mass
44
Cortisol is a pleiotropic hormone. What are some of its affects on bone?
- Decrease bone formation | - Increase bone resorption
45
Cortisol is a pleiotropic hormone. What are some of its affects on CT?
Decrease CT
46
Cortisol is a pleiotropic hormone. What are some of its affects on inflammation/immune system?
*Inhibit inflammatory/immune responses
47
Cortisol is a pleiotropic hormone. What are some of its affects on the CV system?
- Maintain CO - Increase arteriole tone - Decrease endothelial permeability
48
Cortisol is a pleiotropic hormone. What are some of its affects on pregnancy?
Facilitate maturation of the fetus
49
Cortisol is a pleiotropic hormone. What are some of its affects on the kidney?
- Increase GFR | - Increase free water clearance
50
Cortisol is a pleiotropic hormone. What are some of its affects on brain/mood?
Modulate emotional tone, wakefulness
51
What are cortisol's effects on metabolism? (How is it closely related to another important metabolic hormone?) - state how it affects sugar, lipids, protein, Ca2+
Metabolic Actions – potent counter-regulatory hormone to insulin. (antagonizes insulin action) - Mobilizes energy stores: increase plasma glucose = “glucocorticoid” (cortex of adrenal) - Increase GNG and plasma glucose levels - Increase lipolysis - Breaks down muscle protein - proteolysis - *Redistributes fat – abdominal obesity, depletion of subcutaneous fat - Inhibits intestinal calcium absorption
52
What are the 3 enzymes gluconeogenic enzymes that cortisol stimulates the production of?
- Glucose-6-phosphatase - PEP carboxykinase - Tyrosine aminotransferase (malate shuttle)
53
What is the molecular mechanism that regulate insulin antagonism by cortisol in myocytes?
*Decrease GLUT-4 receptors on their membrane (decreases glucose uptake in muscle cells to maintain plasma glucose)
54
In terms of gene TS, how does cortisol affect muscle cells? (should prob memorize)
- Cortisol increases TS of MuRF-1 (an E3 ubiquitin ligase), stimulating proteolysis - Cortisol simultaneously inhibits AA uptake and AKT-P'lation, resulting in decreased protein synthesis
55
How does cortisol stimulate lipolysis in adipose tissue? (3 genes + 1 other function that affect appearance)
1. Increases TS of Mg11 gene- MAG lipase 2. Increases TS of Lipe gene- HSTL 3. Increases TS of Angpt14 gene- increases cAMP and activates HSLT 4. Redistributes fat stores (abdominal obesity, thinning of limbs due to loss of sub-Q fat)
56
By what cellular mechanism to glucocorticoids inhibit inflammation? (anti-inflammatory effects are the primary reason glucocorticoids are given)
GR increases IκB transcription, preventing NF-κB nuclear translocation and thus blocking TS of inflammatory cytokines
57
Besides blocking the synthesis of pro-inflammatory cytokines such as prostaglandins, how else do glucocorticoids affect the immune system and the blood?
- Stimulates anti-inflammatory cytokines - Suppresses AB production - Increases neutrophils, platelets, and RBCs.
58
By what process does cortisol affect intestinal Ca?
Inhibits intestinal Ca2+ absorption thru transcellular transport
59
By what process does cortisol affect bone Ca? (2 ways)
- Inhibits bone formation by decreasing IGF-I receptors | - Increases bone resorption by activating osteoclasts
60
What is the general reasoning behind cortisol's effects on blood flow to the brain/heart?
During physical stress, want blood to flow to brain/heart, away from periphery.
61
Besides shunting blood to the brain/heart, what (3) effects does cortisol have on the vasculature?
- Stimulates red blood cell production - Maintains responsiveness to catecholamine pressor effects (constrict peripheral vessels via alpha-adrenergic receptors; dilate coronary arteries in heart via beta-adrenergic receptors; Glucocorticoid excess = increased blood pressure/HTN) - Maintains vascular integrity and reactivity
62
What psychiatric conditions could stimulate cortisol release?
Depression, anxiety, nervousness, panic, rage/aggression
63
What defines Cushing disease vs Cushing syndrome?
- “Cushing disease” – excessive cortisol secretion due to pituitary adenoma - “Cushing syndrome” – all other excess glucocorticoid etiologies
64
What are the major sx of Cushing dz/syndrome?
- Change in body fat distribution: moon face, buffalo hump, abdominal obesity, thin skin, bruising - Inhibition of intestinal Ca2+ absorption: osteoporosis - Hypertension: excess glucocorticoids activate MR - Glucose intolerant: antagonism of insulin action - Purple Striae – Fragile thin skin stretches over increased abdominal fat, vessels hemorrhage into striae
65
What is the most common cause of Cushing syndrome?
Long-term glucocorticoid therapy
66
What are some eg's where you would use glucocorticoid therapy?
Medical Emergencies: | High acute dose to treat septic shock, severe asthma, severe autoimmune disease flare
67
What are the long-term side effects of glucocorticoids?
None
68
What is the danger of giving too much exogenous cortisol?
Lots of negative feedback…cells die and atrophy, pts no longer make their own glucocorticoids (Therefore pts must be weaned off slowly)
69
What are some effects of chronic glucocorticoid administration, in terms of inflammation? The immune system? The adrenal gland? Pre-term infants?
- Anti-inflammatory - Immunosuppressive - Adrenal insufficiency - Pre-term infants – improved lung function
70
Which of the following glucocorticoids has the strongest potency and is therefore mainly used for diagnositcs? Cortisol, prednisone, dexamethasone, methylprednisone, fludrocortisone
Dexamethasone
71
Which of the following glucocorticoids has the weakest potency? Cortisol, prednisone, dexamethasone, methylprednisone, fludrocortisone
Cortisol
72
What is adrenal insufficiency (AI)? | What are the names of the 2 types?
Failure of adrenal to secrete glucocorticoids, mineralocorticoids, or both - Primary and secondary
73
What is the difference b/w primary and secondary adrenal insufficiency?
- Primary: failure at the adrenal gland | - Secondary: failure to secrete ACTH or CRH
74
Is Addison's dz a primary or secondary adrenal insufficiency?
Primary: autoimmune destruction of adrenals | 70% of primary AI cases
75
What's the most common cause of secondary adrenal insufficiency?
*Sudden cessation of glucocorticoid therapy

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